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EC number: 236-704-1 | CAS number: 13465-77-5
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Endpoint summary
Administrative data
Key value for chemical safety assessment
Effects on fertility
Description of key information
No reproductive toxicity studies are available for hexachlorodisilane,
therefore good quality data for the condensed hydrolysis product,
polysilicic acid (equivalent to SAS) have been read-across.
In a 2-generation reproductive toxicity study (Wolterbeek et al. 2015)
conducted according to OECD TG416 and GLP, Wistar rats were administered
SAS (described as NM-200 synthetic amorphous silica) (in highly
deionised water containing 10% fetal bovine serum) at doses of 100, 300
and 1000 mg/kg bw/day by oral gavage. The dosing schedule and
investigations were conducted according to the OECD TG. There were no
adverse findings in parental animals or offspring in any generation.
Therefore the NOAEL for general toxicity and reproductive toxicity was
≥1000 mg/kg bw/day.
Effect on fertility: via oral route
- Endpoint conclusion:
- no adverse effect observed
- Dose descriptor:
- NOAEL
- 1 000 mg/kg bw/day
- Study duration:
- subchronic
- Species:
- rat
- Quality of whole database:
- The key study was conducted according to OECD TG 416 and to GLP, without any significant deviations, and is therefore a suitable key study.
Effect on fertility: via inhalation route
- Endpoint conclusion:
- no study available
Effect on fertility: via dermal route
- Endpoint conclusion:
- no study available
Additional information
- 150 mg/l ‘SiO2 equivalent’ at pH 2.0 and pH 3.0
- 130 mg/l ‘SiO2 equivalent’ at pH 4.2
- 110 mg/l ‘SiO2 equivalent’ at pH 5.7
- 100 mg/l ‘SiO2 equivalent’ at pH 7.7
- 490 mg/l ‘SiO2 equivalent’ at pH 10.3
- 1120 mg/l ‘SiO2 equivalent’ at pH 10.6
- 120 mg/l ‘SiO2 equivalent’ at pH 2.0
- 150 mg/l ‘SiO2 equivalent’ at pH 7.0
- 170 mg/l ‘SiO2 equivalent’ at 35 °C
- 270 mg/l ‘SiO2 equivalent’ at 65 °C
- 465 mg/l ‘SiO2 equivalent’ at 95 °C
There are no adequate reproductive toxicity data on hexachlorodisilane so good quality data for the hydrolysis products polysilicic acid (equivalent to synthetic amorphous silica) have been used to assess the potential for adverse effects on fertility following exposure to hexachlorodisilane.
Overview
It is considered not to be either ethical or technically feasible to perform reproductive toxicity testing with hexachlorodisilane by any route of exposure due to its known corrosive properties, which dominate the toxicity profile of this substance. Following repeated oral dosing, the corrosive nature of the product could affect the lining of the stomach, giving rise to hyperplasia and a subsequent reduced food intake. This would confound the interpretation of any systemically driven effects. A guideline-compliant repeated-dose inhalation study should elicit systemic toxicity at the highest test concentration. Since the local corrosive effects of hexachlorodisilane would be significant a valid inhalation study according to the relevant guidelines is technically not feasible to do. It is also unlikely that any systemic effects would be seen at dose levels made sufficiently low (< 10 ppm) to prevent the known corrosive effects and/or distress in the test species. This has been confirmed in a 28-day inhalation study with another chlorosilane, dichloro(dimethyl)silane (WIL, 2014) in which there were no effects of treatment on clinical signs, body weight or food consumption that would indicate a systemic effect. Furthermore, the histopathology in the study indicated that the effects in the upper respiratory tract were similar to HCl. It is therefore concluded that HCl will dominate the inhalation toxicity profile of hexachlorodisilane.
With regard to the dermal and inhalation routes, due to the known corrosive effects of hexachlorodisilane, appropriate H-phrases and P-statements are included in the labelling, meaning that repeated skin and inhalation exposure is not expected. Any accidental skin contact or inhalation exposure could cause severe local effects but would be unlikely to cause any systemic effects.
ORAL ROUTE
SYSTEMIC EFFECTS
There are no adequate reproductive toxicity data on hexachlorodisilane so good quality data for synthetic amorphous silica (CAS 112926-00-8) have been used to assess the reproductive toxicity of hexachlorodisilane.
Hexachlorodisilane, like all inorganic chlorosilanes, is a severely corrosive substance that is decomposed by water. The reaction is highly exothermic (Merck, 2013). The estimated half-lives of the substance at 25ºC and pH 4, 7 and 9 are approximately 5 seconds, producing hexahydroxydisilane and hydrogen chloride. Further hydrolysis of the Si-Si bonds in hexahydroxydisilane is expected to happen rapidly and produces monosilicic acid.
Monosilicic acid condenses to insoluble polysilicic acid [equivalent to synthetic amorphous silica (SAS)] at concentrations higher than 100-150 mg/l ‘SiO2equivalent’ in water (Holleman-Wiberg, 2001). At very high concentration, polysilicic acid can condense to silicon dioxide (SiO2). Hexahydroxydisilane is also likely to form condensation products (polyhydroxy-polysilanes) at similar concentrations (in terms of SiO2 equivalents). The structure and predicted properties of the Si-Si containing hydrolysis products (polyhydroxy-polysilanes) and (poly)silicic acid are very similar, and distinguishing between them would be very difficult analytically.The hydrolysis products of hydrochloric acid and (poly)silicic acid are significant for the chemical safety assessment (CSR).
Monosilicic acid and polysilicic acid are naturally occurring substances which are ubiquitous in the environment. Soluble monosilicic acid is the major bioavailable form of silicon and plays an important role in the biogeochemical cycle of silicon (ECETOC, 2006). Typical background concentrations of monosilicic acid in the environment are up to 75 mg/l ‘SiO2 equivalent’ in river water and up to 14 mg/l ‘SiO2equivalent’ in seawater (Iler, 1979).
The literature gives various values for the solubility of silicic acid, determined indirectly as ‘SiO2 equivalent’ because the soluble species cannot be directly measured:
The solubility of monosilicic acid according to Alexander et al. (1954) at 25 °C:
The solubility of monosilicic acid according to Goto and Okura (1953) at 25 °C:
The solubility of monosilicic acid according to Elmer and Nordberg (1958) at neutral pH:
With the described properties of hexachlorodisilane in mind it is not possible to conduct reproductive toxicity studies in experimental animals due to the corrosive nature of this substance. Nor can the hydrolysis product, monosilicic acid, be tested as it is not possible to isolate this substance. However, we know from physicochemical properties that following ingestion of hexachlorodisilane, the conditions in the stomach are such that following an initial rapid hydrolysis to soluble monosilicic acid, this monomer will start to condense to form insoluble polysilicic acid (equivalent to SAS). This condensation will start to occur once the concentration of monosilicic acid reaches approximately 150 mg/l in the gastric juices.
Monosilicic acid (soluble silica) undergoes condensation reactions in solution at about 100-150 mg/l ‘SiO2 equivalent’. The solubility of monosilicic acid in water is 150 mg/l ‘SiO2 equivalent'.
Following dosing by oral gavage, partitioning will occur between the dose vehicle and the aqueous environment in the stomach.
Mass dosed (in mg/day) = Body weight (in kg) x dose level (in mg/kg bw/day)
Dose concentration (in mg/l) = mass dosed (in mg/day)÷volume (in l)
So, the dose level (mg/kg bw/day) required to reach the dose concentration of 150 mg/l 'SiO2 equivalent', the estimated (conservative) maximum concentration of silicic acid that can occur in the stomach before condensation to insoluble polysilicic acid (equivalent to SAS) begins is calculated as follows:
Body weight of rat = 0.3kg
Dose level = X
Estimated aqueous volume = 0.0015 l
Dose concentration = 150 mg/l
150 mg/l = 0.3 kg x dose level (mg/kg bw/day)÷0.0015l
Dose level = 0.75 mg/kg bw/day 'SiO2equivalent'
Therefore based on a condensation limit of 150 mg/l, the maximum dose level that could be used in practice to ensure exposure mainly to monosilicic acid in the stomach of experimental animals is approximately 0.75 mg/kg bw/day or less of 'SiO2 equivalent'.
A correction for molecular weight gives a maximum dose level for hexachlorodisilane:
Mr [hexachlorodisilane] = 268.89 g/mol
Mr [silicon dioxide] = 60.08 g/mol
Dose level [hexachlorodisilane] = [Dose level [silicon dioxide] x Mr [hexachlorodisilane]]
Mr [silicon dioxide]
= (0.75 mg/kg bw/day) x (268.89 g/mol)
(60.08 g/mol)
= 3.36 mg/kg bw/day
Therefore based on a condensation limit of 150 mg/l the maximum dose level of hexachlorodisilane that can be dosed to ensure exposure mainly to monosilicic acid is approximately 3 mg/kg bw/day.
For comparison purposes, using the above calculation, the following shows the dose concentrations for the dose levels typically used in experimental animals studies (100, 300 and 1000 mg/kg bw/day).
Body weight = 0.3 kg
Total amount dosed = 30 mg
Estimated aqueous volume = 1.5 ml
Dose concentration = 20,000 mg/l
Body weight = 0.3 kg
Total amount dosed = 90 mg
Estimated aqueous volume = 1.5 ml
Dose concentration = 60,000 mg/l
Body weight = 0.3 kg
Total amount dosed = 300 mg
Estimated aqueous volume = 1.5 ml
Dose concentration = 200,000 mg/l
Therefore dosing at these levels clearly gives a dose concentration in the stomach that far exceeds the dose at which condensation to polysilicic acid (equivalent to SAS) starts to occur. Consequently, the majority of the dose in the stomach will be present as insoluble polysilicic acid (equivalent to SAS). In all cases only approximately 150 mg/l will be present as soluble monosilicic acid.
Overall, it can be concluded that gavaging hexachlorodisilane at doses unlikely to cause local corrosive effects and at doses that give mainly soluble monosilicic acid (2 mg/kg bw/day or less) would be unethical based on animal usage. However, because the vast majority of a gavaged dose will rapidly condense to insoluble polysilicic acid it is appropriate to use toxicology data on SAS to address the potential for oral reproductive toxicity of hexachlorodisilane.
The key study for reproductive toxicity is a 2-generation reproductive toxicity study (Wolterbeek et al. 2015) conducted according to OECD test guideline 416 and in compliance with GLP. Wistar rats were administered SAS (described as NM-200 synthetic amorphous silica) (in highly deionised water containing 10% fetal bovine serum) at doses of 100, 300 and 1000 mg/kg bw/day by oral gavage. There were no adverse findings in parental animals or offspring in any generation. Therefore the NOAEL for general toxicity and reproductive toxicity was ≥1000 mg/kg bw/day in this study.
Limited data are available regarding the reproductive toxicity in animals following oral, dermal or inhalation exposure to hydrogen chloride. However, protons and chloride ions exist as normal constituents of body fluid in animals, hence low concentrations of hydrogen chloride appear not to cause adverse effects in animals. Therefore the hydrolysis product of hexachlorodisilane, HCl, would not be expected to cause reproductive toxicity in experimental animals or humans following initial exposure to hexachlorodisilane.
References
Alexander G.B., Heston W.M. and Iler R.K. (1954) J. Phys. Chem., 58, 453.
Cotton F.A. and Wilkinson G. (1999) Advanced Inorganic Chemistry, 6thEdition, p271
ECETOC (2006) Synthetic Amorphous Silica (CAS No. 7631-86-9), JACC REPORT No. 51
Elmer and Nordberg (1958) J. Am.Chem. Soc., 41, 517
Goto K. and Okura T. (1953) Kagaku, 23, 426.
Holleman-Wiberg, (2001) Inorganic Chemistry, Academic Press, p. 865
Iler, Ralph K. (1979) The Chemistry of Silica: Solubility, Polymerization, Colloid and Surface Properties and Biochemistry of Silica, Wiley, p. 13.
Jones, R. G., Wataru, A., and Chojnowski, J. (2000) Silicon-Containing Polymers: The Science and Technology of Their Synthesis, Kluwer Academic Press pp168-169
Merck Index (2013) Monograph Number. 8639 (15th Ed)
Effects on developmental toxicity
Description of key information
No developmental toxicity studies are available for hexachlorodisilane, therefore good quality data for the condensed hydrolysis product, polysilicic acid (equivalent to SAS) have been read-across. In a prenatal developmental study (Hofmann et al., 2015) conducted according to OECD TG 414 and to GLP, pregnant Wistar rats were administered SAS (described as NM-200 synthetic amorphous silica) (in highly deionised water containing 10% fetal bovine serum) at doses of 100, 300 and 1000 mg/kg bw/day by oral gavage on gestation days 6-19. The dosing schedule and investigations were conducted according to the OECD TG. There were no adverse, treatment-related findings in parental animals or offspring. There were a number of incidental fetal malformations and variations, which all occurred at a rate no larger than that of the control/historical controls, without statistical significance and without a dose-response relationship. Therefore the NOAEL for general toxicity and developmental (including teratogenicity) toxicity was ≥1000 mg/kg bw/day.
Effect on developmental toxicity: via oral route
- Endpoint conclusion:
- no adverse effect observed
- Dose descriptor:
- NOAEL
- 1 000 mg/kg bw/day
- Study duration:
- subacute
- Species:
- rat
- Quality of whole database:
- The key study was conducted according to OECD TG 414 and to GLP, without any significant deviations, and is therefore a suitable key study.
Effect on developmental toxicity: via inhalation route
- Endpoint conclusion:
- no study available
Effect on developmental toxicity: via dermal route
- Endpoint conclusion:
- no study available
Additional information
- 150 mg/l ‘SiO2 equivalent’ at pH 2.0 and pH 3.0
- 130 mg/l ‘SiO2 equivalent’ at pH 4.2
- 110 mg/l ‘SiO2 equivalent’ at pH 5.7
- 100 mg/l ‘SiO2 equivalent’ at pH 7.7
- 490 mg/l ‘SiO2 equivalent’ at pH 10.3
- 1120 mg/l ‘SiO2 equivalent’ at pH 10.6
- 120 mg/l ‘SiO2 equivalent’ at pH 2.0
- 150 mg/l ‘SiO2 equivalent’ at pH 7.0
- 170 mg/l ‘SiO2 equivalent’ at 35 °C
- 270 mg/l ‘SiO2 equivalent’ at 65 °C
- 465 mg/l ‘SiO2 equivalent’ at 95 °C
There are no adequate developmental toxicity data on hexachlorodisilane so good quality data for the hydrolysis products polysilicic acid (equivalent to synthetic amorphous silica) have been used to assess the potential for adverse effects on development following exposure to hexachlorodisilane.
Overview
It is considered not to be either ethical or technically feasible to perform developmental toxicity testing with hexachlorodisilane by any route of exposure due to its known corrosive properties, which dominate the toxicity profile of this substance. Following repeated oral dosing, the corrosive nature of the product could affect the lining of the stomach, giving rise to hyperplasia and a subsequent reduced food intake. This would confound the interpretation of any systemically driven effects. A guideline-compliant repeated-dose inhalation study should elicit systemic toxicity at the highest test concentration. Since the local corrosive effects of hexachlorodisilane would be significant a valid inhalation study according to the relevant guidelines is technically not feasible to do. It is also unlikely that any systemic effects would be seen at dose levels made sufficiently low (< 10 ppm) to prevent the known corrosive effects and/or distress in the test species. This has been confirmed in a 28-day inhalation study with another chlorosilane, dichloro(dimethyl)silane (WIL, 2014) in which there were no effects of treatment on clinical signs, body weight or food consumption that would indicate a systemic effect. Furthermore, the histopathology in the study indicated that the effects in the upper respiratory tract were similar to HCl. It is therefore concluded that HCl will dominate the inhalation toxicity profile of hexachlorodisilane.
With regard to the dermal and inhalation routes, due to the known corrosive effects of hexachlorodisilane, appropriate H-phrases and P-statements are included in the labelling, meaning that repeated skin and inhalation exposure is not expected. Any accidental skin contact or inhalation exposure could cause severe local effects but would be unlikely to cause any systemic effects.
ORAL ROUTE
SYSTEMIC EFFECTS
There are no adequate developmental toxicity data on hexachlorodisilane so good quality data for synthetic amorphous silica (CAS 112926-00-8) have been used to assess the developmental toxicity of hexachlorodisilane. Local effects from the hydrolysis product, hydrogen chloride (HCl) are not addressed by these data.
Hexachlorodisilane, like all inorganic chlorosilanes, is a severely corrosive substance that is decomposed by water. The reaction is highly exothermic (Merck, 2013). The estimated half-lives of the substance at 25ºC and pH 4, 7 and 9 are approximately 5 seconds, producing hexahydroxydisilane and hydrogen chloride. Further hydrolysis of the Si-Si bonds in hexahydroxydisilane is expected to happen rapidly and produces monosilicic acid.
Monosilicic acid condenses to insoluble polysilicic acid [equivalent to synthetic amorphous silica (SAS)] at concentrations higher than 100-150 mg/l ‘SiO2equivalent’ in water (Holleman-Wiberg, 2001). At very high concentration, polysilicic acid can condense to silicon dioxide (SiO2). Hexahydroxydisilane is also likely to form condensation products (polyhydroxy-polysilanes) at similar concentrations (in terms of SiO2equivalents). The structure and predicted properties of the Si-Si containing hydrolysis products (polyhydroxy-polysilanes) and (poly)silicic acid are very similar, and distinguishing between them would be very difficult analytically.The hydrolysis products of hydrochloric acid and (poly)silicic acid are significant for the chemical safety assessment (CSR).
Monosilicic acid and polysilicic acid are naturally occurring substances which are ubiquitous in the environment. Soluble monosilicic acid is the major bioavailable form of silicon and plays an important role in the biogeochemical cycle of silicon (ECETOC, 2006). Typical background concentrations of monosilicic acid in the environment are up to 75 mg/l ‘SiO2 equivalent’ in river water and up to 14 mg/l ‘SiO2 equivalent’ in seawater (Iler, 1979).
The literature gives various values for the solubility of silicic acid, determined indirectly as ‘SiO2 equivalent’ because the soluble species cannot be directly measured:
The solubility of monosilicic acid according to Alexander et al. (1954) at 25 °C:
The solubility of monosilicic acid according to Goto and Okura (1953) at 25 °C:
The solubility of monosilicic acid according to Elmer and Nordberg (1958) at neutral pH:
With the described properties of hexachlorodisilane in mind it is not possible to conduct developmental toxicity studies in experimental animals due to the corrosive nature of this substance. Nor can the hydrolysis product, monosilicic acid, be tested as it is not possible to isolate this substance. However, we know from physicochemical properties that following ingestion of hexachlorodisilane, the conditions in the stomach are such that following an initial rapid hydrolysis to soluble monosilicic acid, this monomer will start to condense to form insoluble polysilicic acid (equivalent to SAS). This condensation will start to occur once the concentration of monosilicic acid reaches approximately 150 mg/l in the gastric juices.
Monosilicic acid (soluble silica) undergoes condensation reactions in solution at about 100 -150 mg/l ‘SiO2 equivalent’. The solubility of monosilicic acid in water is 150 mg/l ‘SiO2 equivalent'.
Following dosing by oral gavage, partitioning will occur between the dose vehicle and the aqueous environment in the stomach.
Mass dosed (in mg/day) = Body weight (in kg) x dose level (in mg/kg bw/day)
Dose concentration (in mg/l) = mass dosed (in mg/day)÷volume (in l)
So, the dose level (mg/kg bw/day) required to reach the dose concentration of 150 mg/l 'SiO2 equivalent', the estimated (conservative) maximum concentration of silicic acid that can occur in the stomach before condensation to insoluble polysilicic acid (equivalent to SAS) begins is calculated as follows:
Body weight of rat = 0.3kg
Dose level = X
Estimated aqueous volume = 0.0015 l
Dose concentration = 150 mg/l
150 mg/l = 0.3 kg x dose level (mg/kg bw/day)÷0.0015l
Dose level = 0.75 mg/kg bw/day 'SiO2 equivalent'
Therefore based on a condensation limit of 150 mg/l, the maximum dose level that could be used in practice to ensure exposure mainly to monosilicic acid in the stomach of experimental animals is approximately 0.75 mg/kg bw/day or less of 'SiO2 equivalent'.
A correction for molecular weight gives a maximum dose level for hexachlorodisilane:
Mr [hexachlorodisilane] = 268.89 g/mol
Mr [silicon dioxide] = 60.08 g/mol
Dose level [hexachlorodisilane] = [Dose level [silicon dioxide] x Mr [hexachlorodisilane]]
Mr [silicon dioxide]
= (0.75 mg/kg bw/day) x (268.89 g/mol)
(60.08 g/mol)
= 3.36 mg/kg bw/day
Therefore based on a condensation limit of 150 mg/l the maximum dose level of hexachlorodisilane that can be dosed to ensure exposure mainly to monosilicic acid is approximately 3 mg/kg bw/day.
For comparison purposes, using the above calculation, the following shows the dose concentrations for the dose levels typically used in experimental animals studies (100, 300 and 1000 mg/kg bw/day).
Body weight = 0.3 kg
Total amount dosed = 30 mg
Estimated aqueous volume = 1.5 ml
Dose concentration = 20,000 mg/l
Body weight = 0.3 kg
Total amount dosed = 90 mg
Estimated aqueous volume = 1.5 ml
Dose concentration = 60,000 mg/l
Body weight = 0.3 kg
Total amount dosed = 300 mg
Estimated aqueous volume = 1.5 ml
Dose concentration = 200,000 mg/l
Therefore dosing at these dose levels clearly gives a dose concentration in the stomach that far exceeds the dose at which condensation to polysilicic acid (equivalent to SAS) starts to occur. Consequently, the majority of the dose in the stomach will be present as insoluble polysilicic acid (equivalent to SAS). In all cases only approximately 150 mg/l will be present as soluble monosilicic acid.
Overall, it can be concluded that gavaging hexachlorodisilane at doses unlikely to cause local corrosive effects and at doses that give mainly soluble monosilicic acid (2 mg/kg bw/day or less) would be unethical based on animal usage. However, because the vast majority of a gavaged dose will rapidly condense to insoluble polysilicic acid it is appropriate to use toxicology data on SAS to address the potential for oral toxicity of hexachlorodisilane.
The key developmental study is a prenatal developmental study (Hofmann et al., 2015) conducted according to OECD test guideline 414 and in compliance with GLP. Pregnant Wistar rats were administered SAS (described as NM-200 synthetic amorphous silica) (in highly deionised water containing 10% fetal bovine serum) at doses of 100, 300 and 1000 mg/kg bw/day by oral gavage on gestation days 6-19. There were no adverse, treatment-related findings in parental animals or offspring. There were a number of incidental fetal malformations and variations, which all occurred at a rate no larger than that of the control/historical controls, without statistical significance and without a dose-response relationship. Therefore the NOAEL for general toxicity and developmental (including teratogenicity) toxicity was ≥1000 mg/kg bw/day in this study.
Limited data are available regarding the developmental toxicity in animals following oral, dermal or inhalation exposure to hydrogen chloride. However, protons and chloride ions exist as normal constituents of body fluid in animals, hence low concentrations of hydrogen chloride appear not to cause adverse effects in animals. Therefore the hydrolysis product of hexachlorodisilane, HCl, would not be expected to cause developmental toxicity in experimental animals or humans following initial exposure to hexachlorodisilane.
References
Alexander G.B., Heston W.M. and Iler R.K. (1954) J. Phys. Chem., 58, 453.
Cotton F.A. and Wilkinson G. (1999) Advanced Inorganic Chemistry, 6thEdition, p271
ECETOC (2006) Synthetic Amorphous Silica (CAS No. 7631-86-9), JACC REPORT No. 51
Elmer and Nordberg (1958) J. Am.Chem. Soc., 41, 517
Goto K. and Okura T. (1953) Kagaku, 23, 426.
Holleman-Wiberg, (2001) Inorganic Chemistry, Academic Press, p. 865
Iler, Ralph K. (1979) The Chemistry of Silica: Solubility, Polymerization, Colloid and Surface Properties and Biochemistry of Silica, Wiley, p. 13.
Jones, R. G., Wataru, A., and Chojnowski, J. (2000) Silicon-Containing Polymers: The Science and Technology of Their Synthesis, Kluwer Academic Press pp168-169
Merck Index (2013) Monograph Number. 8639 (15th Ed)
Justification for classification or non-classification
Based on the available read-across data from the hydrolysis products insoluble polysilicic acid [equivalent to synthetic amorphous silica (SAS)], hexachlorodisilane does not require classification for toxicity to reproduction according to Regulation (EC) No. 1272/2008.
Additional information
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.
Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.